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. 2016 Dec 5;6:9. doi: 10.1038/s41598-016-0002-7

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© The Author(s) 2016

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Two possible mechanisms for induction of NO synthesis by atropine, suggested by the results reported in this paper. TOP: In the direct pathway, atropine could cause excitation (depolarization) of a target cell; this would cause an increase in intracellular calcium, and possibly activation of nNOS or eNOS – thus leading to NO synthesis and release, and prevention of myopia. BOTTOM: In an indirect pathway, atropine could cause inhibition of a target cell that releases inhibitory transmitters – causing decreased release of neurotransmitter, and thus excitation of the cell that was being inhibited (disinhibition) – finally leading to an increase in intracellular calcium, activation of constitutively expressed nNOS or eNOS, induction of NO synthesis, and prevention of myopia. Each step could represent the overall function of more complex pathway.